Evidence map›Paper›PMID 25994490›Full record

ArticleJournal of neuroinflammation2015

The role of PPAR activation during the systemic response to brain injury.

Patrick Losey, Emma Ladds, Maud Laprais, Borna Guevel, Laura Burns, Regis Bordet, Daniel C Anthony

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Lipophagy and lipid droplets in neurodegeneration.Trends in pharmacological sciences · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Patrick LoseyDepartment of Pharmacology, Experimental Neuropathology, University of Oxford, Mansfield Road, Oxford, OX1 3QT, UK.
Emma LaddsNorth Bristol NHS Trust, Southmead Road, Bristol, BS10 5NB, UK.
Maud LapraisEA 1046, Pharmacology, Faculty of Medicine, Research Branch, IMPRT, University of Lille North of France, Place de Verdun, Lille, Cedex, 59045, France.
Borna GuevelDepartment of Pharmacology, Experimental Neuropathology, University of Oxford, Mansfield Road, Oxford, OX1 3QT, UK.
Laura BurnsDepartment of Pharmacology, Experimental Neuropathology, University of Oxford, Mansfield Road, Oxford, OX1 3QT, UK.
Regis BordetEA 1046, Pharmacology, Faculty of Medicine, Research Branch, IMPRT, University of Lille North of France, Place de Verdun, Lille, Cedex, 59045, France. regis.bordet@univ-lille2.fr.
Daniel C AnthonyDepartment of Pharmacology, Experimental Neuropathology, University of Oxford, Mansfield Road, Oxford, OX1 3QT, UK. daniel.anthony@pharm.ox.ac.uk.
Université de Lille · FRUniversity of Oxford · GBNorth Bristol NHS Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFenofibrate, a PPAR-α activator, has shown promising results as a neuroprotective therapy, with proposed anti-inflammatory and anti-oxidant effects. However, it displays poor blood-brain barrier permeability leading to some ambiguity over its mechanism of action. Experimentally induced brain injury has been shown to elicit a hepatic acute phase response that modulates leukocyte recruitment to the injured brain. Here, we sought to discover whether one effect of fenofibrate might include the suppression of the acute phase response (APR) following brain injury.

methodsA 1-h intraluminal thread middle cerebral artery occlusion (MCAO) model followed by a 6-h reperfusion was performed in C57/BL6 mice. Quantitative reverse transcriptase-polymerase chain reaction was then used to measure hepatic expression of chemokine (C-X-C motif) ligand 1 (CXCL1), chemokine ligand 10 (CXCL10) and serum amyloid A-1 (SAA-1), and immunohistochemical analysis was used to quantify brain and hepatic neutrophil infiltration following stroke.

resultsThe MCAO and sham surgery induced the expression of all three acute phase reactants. A 14-day fenofibrate pre-treatment decreased reactant production, infarct volume, and neutrophil recruitment to the brain and liver, which is a hallmark of the APR.

conclusionsThe data highlight a novel mechanism of action for fenofibrate and lend further evidence towards the promotion of its use as a prophylactic therapy in patients at risk of cerebral ischaemia. Further research is required to elucidate the mechanistic explanation underlying its actions.

Indexed as

Analysis of VarianceAnimalsBrain InjuriesChemokine CXCL1Chemokine CXCL10Disease Models, AnimalFenofibrateInfarction, Middle Cerebral ArteryMaleMiceMice, Inbred C57BLNeuroprotective AgentsNeutrophil InfiltrationPeroxisome Proliferator-Activated ReceptorsRatsRats, WistarChemokine CXCL1Chemokine CXCL10Cxcl10 protein, mouseCxcl1 protein, mouseFenofibrateNeuroprotective AgentsPeroxisome Proliferator-Activated ReceptorsRNA, MessengerSaa4 protein, mouseSerum Amyloid A Protein

Identifiers

PMID25994490
PMCPMC4450490
OpenAlexW1578899206

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.